The recovery of normal function after neural damage is a research area of interest both to clinicians and to basic scientists. We have developed a system to study this problem in the rat pineal gland using the known dependence of the activity of the enzyme serotonin N-acetyltransferase (NAT) on sympathetic nerve activity to measure changes in synaptic stimulation. We have observed that following unilateral denervation of the pineal gland, a midline structure innervated by both superior cervical ganglia, NAT activity is initially greatly depressed. However, within 32 h normal levels of enzyme activity are restored. In contrast, following unilateral decentralization of the superior cervical ganglion, no recovery of pineal function is seen. We propose to study the mechanism of the rapid recovery of pineal function after partial denervation. We will examine the possible roles of 1) loss of norepinephrine uptake sites, 2) increased post-junctional supersensitivity, 3) increases in neural firing in the remaining neurons, and 4) collateral sprouting. Based on available data, we believe the latter three factors are not responsible for the recovery, and we have proposed the novel hypothesis that the disappearance of norepinephrine uptake sites in the degenerating neurons increases the effectiveness of the norepinephrine released by the surviving neurons in stimulating their target cells. A similar "reserve stimulatory capacity" may reside in central adrenergic pathways and in other neural systems which use transmitter uptake as the mechanism of transmitter inactivation. In addition to specifically elucidating the mechanism of this rapid recovery process, we propose to use the pineal gland to examine two general questions related to neural plasticity: 1) what is the relevance of post-junctional supersensitivity as measured by application of exogenous agonists to normal synaptic transmission and 2) what are the conditions which provoke collateral sprouting. These studies will increase our knowledge of the mechanisms underlying plasticity in the adult nervous system. As such they will be relevant to our understanding of factors promoting and limiting the recovery of function after neural damage, such as that caused by stroke and trauma.